Data from 3 community based studies of black and white adolescents ("Project Heart," 1987-1999) have shown that youths at high CVD risk who exhibit agonistic (AG) behavior and increased vascular resistance under a structured social challenge have elevated ambulatory blood pressure (ABP) in the natural environment. Evidence suggests that this AG pattern: (a) may be related to increased interpersonal stress and increased risk of CVD (e.g., essential hypertension, metabolic syndrome), and (b) may be exacerbated by a reduced ability to modulate negative affect due to impaired cognitive control and / or parasympathetic control. AG behavior and impaired cognitive / parasympathetic affect modulation (AM) may combine to generate social stress and thereby elevate CVD risk. We now propose to test this model in an adult sample of 240 former Project Heart (PH) participants who now are 24-34 years old. In this well characterized group, we will test hypothesized relationships between the AG pattern, AM (cognitive / parasympathetic) under social challenge, interpersonal conflict (IPC) recorded via electronic diaries, ABP, and metabolic syndrome (fasting glucose, lipids, blood pressure, visceral obesity), in a design that combines new measures of these variables with pooled data obtained earlier at age 14-15. Study 1 (Years 1 - 3) will test the hypothesis that young adults who exhibit the AG pattern and impaired AM under challenge also exhibit more frequent IPC recorded by electronic diary, elevated ABP, and higher levels of metabolic syndrome indices. Secondary analyses will test this model with salivary cortisol and immune markers (C-RP, IL-6) as outcomes. Study 2 (Year 4) will pool data from the 3 original PH studies to generate indices of adolescent AG behavior, AG stress (AS;anger arousal / hostility/ hostile environment), Dysphoric Affect (DA;anxiety/ depression/ isolation), and risky health habits (RHH), for causal models testing the hypothesis that increased IPC stress and CVD risk in young adulthood is associated with increases (from ages 14-15 to ages 24-34) in AS, DA, and RHH. The proposed causal models identify: (a) aspects of persons (e.g., AG behavior, cognitive AM) and social environments (e.g., IPC) that can be modified by preventive intervention, or (b) used to identify subgroups at risk (e.g., due to impaired parasympathetic control), and thus will guide practical public health efforts to reduce CVD risk in minority youth and young adults.